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Pathologies ADULTS > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is a false aneurysm or pseudoaneurysm?

when does it occur?

A

when the two inner layers of the aorta (intima and media) rupture and there dilation of the vessel, with the blood being contained by the outer layer (adventita).

Occurs from trauma or after surgery to aorta or infection in vessels

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2
Q

What true aneurysm?

A

where all 3 layers of aorta is intact but dilated

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3
Q

what is aortic dissection?

A

where blood enters between the intima and media layer

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4
Q

Who are more affected by thoracic aortic aneurysm?

What are some of the other risk factors of thoracic aortic aneurysm?

A

Men and also at younger age than women.

risk factors:

  • increased age
  • smoking
  • hypertension
  • family history
  • Marfan Syndrome or other connective tissue disorder
  • existing cardio disease.
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5
Q

Does dilation of thoracic aorta cause symptoms?

What are the symptoms of thoracic aneurysm due to it taking up space in the mediastinum?

A

No symptoms - only found incidentally.

Symptoms include:

  • Chest or back pain
  • Trachea or left bronchus compression may cause cough, SOB, and stridor.
  • phrenic nerve compression cause hiccups
  • Oesophageal compression cause dysphagia (difficulty swallowing)
  • recurrent laryngeal nerve compression cause hoarse voice
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6
Q

What investigations can be done for the diagnosis of thoracic aortic aneurysm?

A
  • Echocardiogram

- CT or MRI angiogram

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7
Q

Management of thoracic aortic aneurysm?

what would be does if the aneurysm was large

A
  • treat modifiable risk factors (smoking, diet, management of hypertension, diabetes and hyperlipidaemia)

Options vary depending on size, larger is likely to rupture, management options include:

  • Surveillance with regular imaging to monitor the size
  • Thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the aorta
  • Open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft
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8
Q

where does a ruptured thoracic aortic aneurysm bleed into? and what can this cause?

A
  • Oesophagus, causing haematemesis (vomiting blood).
  • Airways or lungs, causing haemoptysis (coughing up blood)
  • Pericardial cavity, causing cardiac tamponade (compression of the heart)
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9
Q

What does ruptured thoracic aortic aneurysm present as?

A
  • severe chest pain or back pain
  • haemodynamic instability (hypotension and tachycardia).
  • Collapse
  • Death (often patients do not reach hospital).
  • Emergency open surgery is required, replace affected area from synthetic graft.
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10
Q

What scoring system is used to calculate the percentage risk of a patient will have stroke or MI, in the next 10 years? What statin is given to patients with above 10% risk? - what are patients are given this statin?

A

QRISK 3 score - if you have more than 10% risk of having stroke or MI in the next 10 years, patients SHOULD start statin - Nice guidelines are for atorvastatin 20mg at night.

Patients with CKD or type 1 diabetes for the 10 years should be offered atorvastatin 20mg.

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11
Q

What are the 4 As for secondary prevention after developing cardiovascular disease?

A
  • Aspirin (plus a second anti-platelet such as clopidogrel for 12 months).
  • Atorvastatin 80mg
  • Atenolol (commonly bisoprolol)
  • ACE inhibitor (commonly ramipril)
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12
Q

What are the notable side effects of statin?

A
  • Myopathy (check creatine kinase in patients with muscle pain or weakness)
  • Type 2 diabetes
  • Haemorrhage strokes (very rarely)
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13
Q

What is an angina?

A

narrowing of the coronary arteries which then reduces blood flow to the myocardium

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14
Q

What is the classic symptom of angina?

A

Constricting chest pain with or without radiation to jaw or arms.

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15
Q

What is stable and unstable angina?

A
  • Stable is when symptoms are relieved by rest or glyceryl trinitrate (GTN).
  • Unstable is when symptoms comes on at rest and is considered as acute coronary syndrome (ACS)
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16
Q

What is the gold started diagnostic investigation for angina?

A

CT coronary angiography.

Also do:
- Physical Examination (heart sounds, signs of heart failure, BMI)

  • ECG
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • Lipid profile
  • Thyroid function tests (check for hypo / hyper thyroid)
  • HbA1C and fasting glucose (for diabetes)
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17
Q

What are the 4 principles to management for angina? RAMP

A

R - refer to cardio urgent
A - advise them about diagnosis, management and call ambulance
M - medical treatment
P - procedural or surgical intervention

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18
Q

Medical management of angina: immediate symptomatic relief

A
  • GTN

repeat after 5 minutes and if still pain repeat after 5 and call ambulance.

19
Q

Medical management of angina: Long term symptomatic relief

A

1) used on its own or in combo if symptoms are not controlled: Beta blocker (e.g. bisoprolol 5mg once daily) or Calcium channel blocker (e.g. amlodipine 5mg once daily).

Other options (not 1st line):

  • Long acting nitrates (e.g. isosorbide mononitrate)
  • Ivabradine
  • Nicorandil
  • Ranolazine
20
Q

Medical management of angina: Secondary prevention

A
  • Aspirin (i.e. 75mg once daily)
  • Atorvastatin 80mg once daily
  • ACE inhibitor
  • Already on a beta-blocker for symptomatic relief.
21
Q

What are the surgical intervention for angina?

A

1) Percutaneous Coronary intervention (PCI) with coronary angioplasty (dilating the blood vessels with a balloon or inserting a stent).
2) Coronary Artery bypass graft (CABG) - for patients with severe stenosis. Takes graft vein from patients leg (great saphenous vein).

Patients with coronary artery disease may have midline sternotomy scar (CABG) or scars around brachial and femoral arteries (PCI)

22
Q

What is Acute coronary syndrome (ACS)?

A

blockage of coronary artery as a result of thrombus from an atherosclerotic plaque. Thrombus formed in fast flowing artery are mostly made of platelets hence the anti-platelet medications

23
Q

The left coronary artery becomes the Circumflex and Left Anterior Descending (LAD), what do these supply?

A

Circumflex artery - Left atrium and posterior aspect of the left ventricle.

Left anterior descending (LAD): anterior aspect of left ventricle and anterior aspect of the septum

24
Q

What does the right coronary artery (RCA) supply?

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area
25
Q

What are the 3 types of ACS?

A
  • unstable angina
  • ST elevation myocardial infarction (STEMI)
  • Non-ST elevation myocardial infarction (NSTEMI)
26
Q

What are the symptoms of ACS?

A

Central, Constricting chest pain associated with:

  • Nausea and vomiting
  • sweating and clamminess
  • feeling of impending doom
  • SOB
  • palpitation
  • Pain radiating to jaws or arm

NOTE symptoms should last 20mins, diabetic patients may not experience chest pain e.g. silent MI

27
Q

ECG changes for STEMI

A
  • ST segment elevation in leads consistent with an area of ischaemia
  • New left Bundle branch block
28
Q

ECG changes for NSTEMI

A
  • ST segment depression in a region
  • Deep T wave inversion
  • Pathological Q waves (suggest deep infarct)
29
Q

Troponin blood tests significance in ACS

A
  • If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
  • If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain
30
Q

What are troponins?

A

They are proteins found in cardiac muscles.

Diagnosis of ACS require serial troponin levels (at baseline and then 6 or 12 hours after onset of symptom).

Rise is consistent with myocardial ischaemia as protein is released from ischaemic muscles.

HOWEVER they are non specific!

31
Q

Other than ACS, what causes raised troponins?

A
  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • PE
32
Q

Other than ECG and troponin levels, what other investigations are performed for ACS?

A

all the ones of angina

plus:
- Chest x ray for other causes of chest pain and pulmonary oedema

  • Echocardiogram after event to check for functional damage
  • CT coronary angiogram - assess for coronary artery disease.
33
Q

What Acute STEMI and what are the treatment options?

A

Acute STEMI is patients with STEMI presenting within 12 hours of onset.

Treatment is either:

  • PCI (removed or aspirate the blockage and stent is put in).
  • Thrombolysis (injecting fibrinolytic medication that rapidly dissolve clot)
34
Q

Some exampled of thrombolytic agents.

A

Streptokinase, Alteplase and Tenecteplase

35
Q

Acute NSTEMI treatment: BATMAN

A

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain

A – Anticoagulant: Fondaparinux (unless high bleeding risk)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

36
Q

What scoring system is used to assess for PCI in NSTEMI? and what do each percentage mean.

A

GRACE score- this system system gives a 6-month risk of death or repeat MI after having an NSTEMI:

<5% Low Risk
5-10% Medium Risk
>10% High Risk

If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

37
Q

What is Dressler’s syndrome? What does it present as?

A

It is a post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis.

Present as pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade.

38
Q

How to make the diagnosis for Dressler’s syndrome? And what is the management?

A

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Management is:

  • NSAIDS
  • severe cases steroids (prednisolone) and may need pericardiocentesis.
39
Q

What is the secondary prevention management for ACS? 6 As

A
  • Aspirin 75mg once daily
  • Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
  • Atorvastatin 80mg once daily
  • ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
  • Atenolol (or other beta blocker titrated as high as tolerated)
  • Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
40
Q

What are the features of Beck’s triad? and what pathology does it indicate?

A

Becks triad - hypotension, raised JVP and muffled heart sounds.

Indicator of cardiac tamponade

41
Q

What ECG sign is seen for hyperkalaemia?

A
  • Tall tented T waves
  • Flattened P waves
  • Broad QRS complex
42
Q

What ECG sign is seen for hypokalaemia?

A
  • Tall P waves
  • U waves
  • T wave depression
43
Q

What ECG sign is seen for Wolfe-Parkinson-White?

A

Delta waves

Pathologies ADULTS (9 decks)

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